It has long been known that β-cell neogenesis, new β-cell formation from non β-cell precursors, could result in expansion of the β-cell mass (1). Only recently has induction of β-cell neogenesis received attention as a therapy for diabetes mellitus. As the wealth of information about β-cell neogenesis increases, general ideals form about the type of tissue and by what means these tissues are involved. Unfortunately, since β-cell neogenesis is a dynamic process, and we can only measure β-cell mass once for each subject, it is not easy to measure β-cell neogenesis. The current hallmark of β-cell neogenesis is endocrine cells budding from ductal structures (2). From an immunohistochemical position, it is very easy to record and quantify duct associated β-cell neogenesis. Because of this, less interest has been focused on the possibility of other pancreatic tissues giving rise to new β-cells.
The adult pancreas is approximately 80-85% acinar tissue, 15-20% duct tissue and 12% endocrine tissue. Based on this tissue division, acinar tissue could potentially be a large source of neogenic β-cell. The same difficulties exist in determining acinar-to-β-cell transdifferentiation as measuring duct-associated neogenesis. However, because islets are not normally found proximal to ducts, duct-associated β-cell neogenesis garners more credibility than acinar-associated β-cell neogenesis, where mature islets are normally found. Since mature islets consist of a central core of β-cells surrounded by a mantel of α, δ and PP cells, one way to quantify acinar-to-β-cell neogenesis is to determine the number of single insulin positive cells or small cell clusters devoid of any other endocrine cells (suggesting recent formation), that are associated with acinar tissue. Likewise, analyzing the co-localization of acinar and endocrine granules can also be used to suggest the occurrence of acinar-to-β-cell neogenesis.